HMGB2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disrupted HMGB2 expression in the Jurkat human T lymphocyte cell line. This loss-of-function model enables detailed investigation of HMGB2??s roles in chromatin remodeling, transcriptional regulation, and immune signaling. The polyclonal format yields a heterogeneous yet consistent knockout pool, eliminating single-cell clonal selection while preserving population-level reproducibility suitable for high-throughput screening and functional assays.
Jurkat cells, an immortalized T lymphocyte line derived from acute T cell leukemia, serve as a widely used model for TCR signaling, apoptosis, and leukemogenesis. Their suspension growth and well-characterized signaling networks make them exceptionally suited for CRISPR-based gene disruption studies. These cells retain core T cell features, including activation-dependent NF-??B and MAPK cascades, while the leukemic background enhances relevance for oncogenic pathway analysis and drug response profiling.
HMGB2 is a non-histone chromosomal protein that acts as a DNA chaperone, modulating nucleosome dynamics, DNA bending, and transcription factor accessibility, and is also an endogenous ligand for pattern-recognition receptors RAGE and TLR4. Its expression is upregulated by TCR engagement, TNF-??, IL-1??, and the transcription factor SP1. Upon activation, HMGB2 signals downstream through RAGE?CMyD88?CIKK?CNF-??B and TLR4 pathways, and it functionally interacts with p53 and MAPK cascades. Consequently, HMGB2 knockout in Jurkat cells impairs these signaling axes, leading to attenuated NF-??B-driven transcription and altered cellular responses to inflammatory and genotoxic stress.
Within the Jurkat T lymphocyte context, HMGB2 disruption reduces TCR- and cytokine-mediated NF-??B activation, thereby compromising proliferation and survival signals critical for leukemic cell maintenance. This model holds particular value for dissecting HMGB2??s contributions to T cell acute lymphoblastic leukemia, sepsis, and autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus, where RAGE/TLR4-mediated signaling drives pathology. Furthermore, a compromised DNA damage response in HMGB2-deficient cells furnishes a platform for interrogating genomic instability and therapy resistance mechanisms.
These polyclonal knockout cells are applicable to mechanistic studies in T cell biology, high-content screening for HMGB2-pathway modulators, and evaluation of immunotherapeutic strategies. Compatible readouts include western blotting and RT-qPCR for target validation, RNA-seq for transcriptomic profiling, flow cytometry for activation markers and apoptosis, NF-??B reporter assays, and cell proliferation measurements. This versatile model is supported by Ascent Research??s technical resources. For further details, please contact Ascent Research.
